| First Author | Agoro R | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 11 | Pages | 2531-2541 |
| PubMed ID | 27569535 | Mgi Jnum | J:247029 |
| Mgi Id | MGI:5922686 | Doi | 10.1002/eji.201646366 |
| Citation | Agoro R, et al. (2016) IL-1R1-MyD88 axis elicits papain-induced lung inflammation. Eur J Immunol 46(11):2531-2541 |
| abstractText | Allergic asthma is characterized by a strong Th2 response with inflammatory cell recruitment and structural changes in the lung. Papain is a protease allergen disrupting the airway epithelium triggering a rapid inflammation with eosinophilia mediated by innate lymphoid cell activation (ILC2) and leading to a Th2 immune response. In this study, we focused on inflammatory responses to a single exposure to papain and showed that intranasal administration of papain results in the recruitment of inflammatory cells, including neutrophils and eosinophils with a rapid production of IL-1alpha, IL-1beta, and IL-33. The inflammatory response is abrogated in the absence of IL-1R1 and MyD88. To decipher the cell type(s) involved in MyD88-dependent IL-1R1/MyD88 signaling, we used new cell-specific MyD88-deficient mice and found that the deletion of MyD88 signaling in single cell types such as T cells, epithelial cells, CD11c-positive or myeloid cells leads to only a partial inhibition compared to complete absence of MyD88, suggesting that several cell types contribute to the response. Importantly, the inflammatory response is largely ST2 and IL-36R independent. In conclusion, IL-1R1 signaling via MyD88 is critical for the first step of inflammatory response to papain. |
